Epigenetic background of neuronal fate determination

Wen, Sijian; Li, Hong; Liu, Jia

doi:10.1016/j.pneurobio.2008.10.002

Cited by 22 publications

(19 citation statements)

References 242 publications

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“…Epigenetic regulation is now emerging as an important cellular mechanism for mediating the interplay between extrinsic and intrinsic signals, such as morphogenic signaling pathways and transcription factor codes, to determine cell type specific gene expression profiles [67], [68]. In fact, REST and CoREST recruit a diverse group of epigenetic factors to their regulatory complexes where they play roles in cell type specific transcriptional regulation and in cell fate determination [11], [15].…”

Section: Resultsmentioning

confidence: 99%

Differential Deployment of REST and CoREST Promotes Glial Subtype Specification and Oligodendrocyte Lineage Maturation

et al. 2009

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BackgroundThe repressor element-1 (RE1) silencing transcription factor/neuron-restrictive silencer factor (REST/NRSF) is a master transcriptional regulator that binds to numerous genomic RE1 sites where it acts as a molecular scaffold for dynamic recruitment of modulatory and epigenetic cofactors, including corepressor for element-1-silencing transcription factor (CoREST). CoREST also acts as a hub for various cofactors that play important roles in epigenetic remodeling and transcriptional regulation. While REST can recruit CoREST to its macromolecular complex, CoREST complexes also function at genomic sites independently of REST. REST and CoREST perform a broad array of context-specific functions, which include repression of neuronal differentiation genes in neural stem cells (NSCs) and other non-neuronal cells as well as promotion of neurogenesis. Despite their involvement in multiple aspects of neuronal development, REST and CoREST are not believed to have any direct modulatory roles in glial cell maturation.Methodology/Principal FindingsWe challenged this view by performing the first study of REST and CoREST in NSC-mediated glial lineage specification and differentiation. Utilizing ChIP on chip (ChIP-chip) assays, we identified distinct but overlapping developmental stage-specific profiles for REST and CoREST target genes during astrocyte (AS) and oligodendrocyte (OL) lineage specification and OL lineage maturation and myelination, including many genes not previously implicated in glial cell biology or linked to REST and CoREST regulation. Amongst these factors are those implicated in macroglial (AS and OL) cell identity, maturation, and maintenance, such as members of key developmental signaling pathways and combinatorial transcription factor codes.Conclusions/SignificanceOur results imply that REST and CoREST modulate not only neuronal but also glial lineage elaboration. These factors may therefore mediate critical developmental processes including the coupling of neurogenesis and gliogenesis and neuronal-glial interactions that underlie synaptic and neural network plasticity and homeostasis in health and in specific neurological disease states.

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Section: Resultsmentioning

confidence: 99%

Differential Deployment of REST and CoREST Promotes Glial Subtype Specification and Oligodendrocyte Lineage Maturation

et al. 2009

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“…During neural ectoderm formation in mammals, various epigenetic factors regulate the activities of external and intracellular signaling pathways and sequential activation/inactivation of fate-determining transcription factors in an orchestrated manner, leading to the transition from the inner cell mass to the epiblast and then to the neural ectoderm (32). Similar events occur during ESC differentiation into neural progenitors (33).…”

Section: Discussionmentioning

confidence: 99%

Epigenetic Regulation of miR-302 by JMJD1C Inhibits Neural Differentiation of Human Embryonic Stem Cells

Wang

Park

Drissi

et al. 2014

Journal of Biological Chemistry

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Background: Histone methylation plays important roles in development and embryonic stem cell (ESC) differentiation. Results: Inhibition of the H3K9 demethylase JMJD1C directly down-regulated miR-302 and promoted neural differentiation of human ESCs (hESCs). Conclusion: JMJD1C inhibits neural differentiation of hESCs at least partially by epigenetically sustaining miR-302 expression. Significance: We provide novel evidence for epigenetic regulation of miR-302 to control neural differentiation of hESCs.

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“…This process, typical of immature stem cells, requires a high biosynthetic activity to produce those intrinsic and external factors that control cell fate by modulating the expression of stage-specific genes (41). Those molecules, involved in the dynamic gene expression control are then silenced in committed NSC derivates by several molecular mechanisms, one of which is the ubiquitin proteasome-dependent pathway.…”

Section: Volume 286 • Number 21 • May 27 2011mentioning

confidence: 99%

mSEL-1L (Suppressor/Enhancer Lin12-like) Protein Levels Influence Murine Neural Stem Cell Self-renewal and Lineage Commitment

Cardano

Diaferia

Cattaneo

et al. 2011

Journal of Biological Chemistry

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Human SEL1L is an endoplasmic reticulum (ER) 3 resident protein (1-3) intensively expressed in neuroepithelial and pancreatic structures (4). Mouse SEL1L (mSEL-1L) was reported to be abundantly represented throughout the neural tube and dorsal root ganglia with higher abundance in the floor plate starting at embryonic day 10.5 (5). Recently, it has been shown that mSEL-1L gene trap mice were embryonic lethal and displayed growth and differentiation impairment of pancreatic epithelial cells (6). This is probably due to a systemic endoplasmic reticulum stress, which activated a defective unfolded protein response and impaired protein degradation (7).SEL1L, in association with HRD1 (E3 ligase), is a key component of the endoplasmic reticulum-associated degradation pathway, acting as a "gate keeper" in the control of newly synthesized soluble and membrane-bound proteins (1, 2). ER quality control mechanisms (8 -10) and proteasome degradation (11) are known to regulate proteins implicated in different cellular processes. Several reports have highlighted the role of ubiquitin ligases and proteasome in neural stem cell self-renewal, survival, and commitment (9, 10). The ubiquitin-proteasome-mediated degradation controls the availability of NSC fundamental proteins, such as Nestin (12), REST (repressor element 1-silencing transcription factor) (13-16), N-Myc (17), and components of the Notch/Delta/Numb pathway (18 -20). Actually, one of the most important goals in stem cell biology is to unravel the mechanisms that control stem cell self-renewal by modulating molecules with key roles in stemness or cell fate choice (21). The proteasomal degradation pathway is a very complicated regulatory network that integrates cell intrinsic and cell extrinsic signals and partially controls the balance between self-renewal and differentiation. In particularly, epigenetic modifiers, no-coding RNA regulators (microRNA: miR-9, let-7b, miR-137, and miR-124) (22), and specific signaling pathways (Notch, FGF, Wnt, Hedgehog, and ␤-catenin) (23) are emerging as a coordinated machinery that manages NSC fate by activating/repressing specific key regulators. In this study, we explored the possible involvement of mSEL-1L in this network. We found that mSEL-1L protein is selectively expressed in pluripotent embryonic stem cells and in multipotent NSCs, acting as a primitive marker of stemness. We also show that mSEL-1L protein expression is finely controlled by fine microRNA regulation both in vivo during mouse embryonic development and in vitro during NSC differentiation. However, its complete depletion heavily affects self-renewal capacity, by negatively regulating those important genes known to maintain the neural progenitor state. The results here presented reaffirm the previously published concept that mSEL-1L is a "multifaced" protein (4), affecting different biochemical pathways.

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Epigenetic background of neuronal fate determination

Cited by 22 publications

References 242 publications

Differential Deployment of REST and CoREST Promotes Glial Subtype Specification and Oligodendrocyte Lineage Maturation

Differential Deployment of REST and CoREST Promotes Glial Subtype Specification and Oligodendrocyte Lineage Maturation

Epigenetic Regulation of miR-302 by JMJD1C Inhibits Neural Differentiation of Human Embryonic Stem Cells

mSEL-1L (Suppressor/Enhancer Lin12-like) Protein Levels Influence Murine Neural Stem Cell Self-renewal and Lineage Commitment

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